Conditioned effects of cocaine are relatively resistant to extinction. Following extinction, conditioned responses can be reinstated with a small priming dose of cocaine. The magnitude of conditioned increases in locomotor activity and stereotypy are dependent on the conditioning dose of cocaine. Injections of cocaine into the n. accumbens are also able to elicit conditioned effects. Unlike cocaine, amphetamine does not appear to support conditioning following one training session. A blockade of glutamate function with MK-801, a noncompetitive antagonist, prevents cocaine-induced conditioning. ECS delivered immediately following a cocaine conditioning session prevents cocaine-induced conditioning. ECS delivered one hour prior and one hour following conditioning or one hour prior to testing was ineffective, illustrating that cocaine-induced conditioning is determined by associative processes. Dopamine depleting lesions of the n. accumbens and amygdala prevent cocaine-induced conditioning. Dopamine depleting lesions of the frontal cortex and striatum were not effective in preventing the conditioned locomotor effects of cocaine. Lesions of the raphe and locus coeruleus were equally ineffective. Stimuli associated with cocaine develop the ability to release mesolimbic dopamine.